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Article first published online: 29 JUN 2007
Copyright © 2007 American Association for the Study of Liver Diseases
Volume 46, Issue 2, pages 388–394, August 2007
How to Cite
Buster, E. H. C. J., Hansen, B. E., Buti, M., Delwaide, J., Niederau, C., Michielsen, P. P., Flisiak, R., Zondervan, P. E., Schalm, S. W. and Janssen, H. L. A. (2007), Peginterferon alpha-2b is safe and effective in HBeAg-positive chronic hepatitis B patients with advanced fibrosis. Hepatology, 46: 388–394. doi: 10.1002/hep.21723
Financial support and study medication provided by Schering-Plough International, Kenilworth, NJ; and GlaxoSmithKline, Research and Development, Greenford, UK.
Monitoring was coordinated by Denys Research Consultants bvba, De Haan, Belgium. Data collection and data management was done by Elke Verhey and Eva Leeuwenhoek, Clinical Research Bureau, Department of Gastroenterology and Hepatology, Erasmus MC, University Medical Center Rotterdam, The Netherlands.
Potential conflict of interest: Nothing to report.
Other members of the HBV 99-01 study group are listed in Acknowledgment.
- Issue published online: 27 JUL 2007
- Article first published online: 29 JUN 2007
- Manuscript Accepted: 8 MAR 2007
- Manuscript Received: 15 JAN 2007
- Schering-Plough International, Kenilworth, NJ
- GlaxoSmithKline, Research and Development, Greenford, UK
- Foundation for Liver Research (SLO), Rotterdam, The Netherlands
Chronic hepatitis B (CHB) patients with advanced fibrosis are often not considered for treatment with peginterferon (PEG-IFN) because IFN therapy may precipitate immunological flares, potentially inducing hepatic decompensation. We investigated the efficacy and safety of treating hepatitis B e antigen (HBeAg)–positive CHB patients with 52 weeks of PEG-IFN-α-2b (100μg weekly) alone or in combination with lamivudine (100 mg daily). Seventy patients with advanced fibrosis (Ishak fibrosis score 4–6) and 169 patients without advanced fibrosis, all with compensated liver disease, participated in the study. Virologic response, defined as HBeAg seroconversion and hepatitis B virus (HBV) DNA < 10,000 copies/ml at week 78, occurred significantly more often in patients with advanced fibrosis than in those without (25% versus 12%, respectively; P = 0.02). Also patients with cirrhosis (n = 24) exhibited a virologic response more frequently than did patients without cirrhosis (30% versus 14%, respectively; P = 0.02). Improvement in liver fibrosis occurred more frequently in patients with advanced fibrosis (66% versus 26%, P < 0.001). HBV genotype A was more prevalent among patients with advanced fibrosis than among those without (57% versus 24%, P < 0.001). Most adverse events, including serious adverse events, were observed equally as frequently in patients with advanced fibrosis and those without. Fatigue, anorexia, and thrombocytopenia occurred more often in patients with advanced fibrosis than in those without (P < 0.01). Necessary dose reduction or discontinuation of therapy was comparable for both patient groups (P = 0.92 and P = 0.47, respectively). Conclusion: PEG-IFN is effective and safe for HBeAg-positive patients with advanced fibrosis. Because PEG-IFN therapy results in a high rate of sustained off-therapy response, patients with advanced fibrosis or cirrhosis but compensated liver disease should not be excluded from PEG-IFN treatment. (HEPATOLOGY 2007.)